BCAR3 (phospho)
breast cancer anti-estrogen resistance 3

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Product Preparation
A synthetic peptide surrounding of –DRTPE- of human BCAR3 protein with a single phosphorylation site. This sequence is identical to human, rat, mouse, canis and bovine.
Background
Breast cancer anti-estrogen resistance 3 (BCAR3) is a also known as AND-34/BCAR3/NSP2 (BCAR3). Breast tumors are initially dependent on estrogens for growth and progression and can be inhibited by anti-estrogens such as tamoxifen. However, breast cancers progress to become anti-estrogen resistant. BCAR3 was identified in the search for genes involved in the development of estrogen resistance. The gene encodes a component of intracellular signal transduction that causes estrogen-independent proliferation in human breast cancer cells. The protein contains a putative src homology 2 (SH2) domain, a hall mark of cellular tyrosine kinase signaling molecules, and is partly homologous to the cell division cycle protein CDC48
PURIFICATION
The Rabbit IgG is purified by site-modified Epitope Affinity Purification.
SPECIFICITY
This antibody recognizes phosphorylated Threonin 130 of human BCAR3 protein. It does not recognize the nonphosphorylated BCAR3.
FORMULATION
This affinity purified antibody is supplied in sterile Tris-buffered saline (pH7.2) containing antibody stabilizer.
STORAGE
The antibodies are stable for 12 months from date of receipt when stored at –20oC. The antibodies can be stored at 2oC-8oC for one month without detectable loss of activity. Avoid repeated freezing-thawing cycles.
Gene ID
8412
Applications/Suggested Working Dilutions
Western Blot
0.1-1 µg/ml
ELISA
0.01-0.1 µg/ml
Immunoprecipitation
2-5 µg/ml
IHC
2-10 µg/ml
Flow cytometry
5-10 µg/ml
Order Info
Catalog #: 600-080
Lot #: See the label
Size: 100 ug
Host: Rabbit
Isotyping: Rabbit IgG
Applications: WB, IHC
Reactivity: Hu, Rt, Ms
Price: $ 330.00
REFERENCES
Makkinje,A., et al. AND-34/BCAR3 regulates adhesion-dependent p130cas serine phosphorylation and breast cancer cell growth pattern. Cell. Signal. 21 (9), 1423-1435 (2009).
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